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Updated: Jun 26, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Negative regulation of SH2B3 by SMYD5 controls epithelial-mesenchymal transition in lung cancer

In Hwan Tae1, Tae Young Ryu1, Yunsang Kang2

  • 1Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea.

Molecules and Cells
|May 9, 2024
PubMed

Insights

Lung cancer metastasis is a major cause of death. Researchers identified SET and MYND domain-containing protein 5 (SMYD5) as a key regulator of lung cancer metastasis, suggesting it as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Metastasis is the primary cause of mortality in lung cancer patients.
  • Identifying novel therapeutic targets to inhibit metastasis is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the role of SET and MYND domain-containing protein 5 (SMYD5) in lung cancer metastasis.
  • To evaluate SMYD5 as a potential therapeutic target for lung cancer treatment.

Main Methods:

  • RNA-sequencing analysis using TCGA data and immunohistochemical analysis to assess SMYD5 expression in lung cancer.
  • SMYD5 knockdown experiments in NCI-H1299 and H1703 cell lines to evaluate effects on cell migration and invasion.
  • Analysis of epithelial-mesenchymal transition markers, MMP9, Src homology 2-b3, and H4K20 trimethylation levels.
  • In vitro epithelial-mesenchymal transition induction using TGF-β.

Main Results:

  • SMYD5 was found to be overexpressed in lung cancer tissues.
  • Knockdown of SMYD5 significantly inhibited cell migration and invasion in lung cancer cell lines.
  • SMYD5 knockdown altered epithelial-mesenchymal transition markers and MMP9 expression.
  • SMYD5 knockdown led to increased Src homology 2-b3 expression by decreasing H4K20 trimethylation.
  • SMYD5 inhibition reduced cell migration and invasion in a TGF-β-induced EMT model.

Conclusions:

  • SMYD5 is identified as a novel regulator of lung cancer metastasis.
  • SMYD5 represents a potential therapeutic target for lung cancer.
  • Combination therapy with SMYD5 inhibitors and chemotherapy may enhance treatment efficacy.
Keywords:
Epithelial-mesenchymal transitionLung cancerMetastasisSMYD5

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